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PubMed1999

Solution structure of a five-adenine bulge loop within a DNA duplex.

The three-dimensional solution structure of a DNA molecule of the sequence 5'-d(GCATCGAAAAAGCTACG)-3' paired with 5'-d(CGTAGCCGATGC)-3' containing a five-adenine bulge loop (dA(5)-bulge) between two double helical stems was determined by 2D (1)H and (31)P NMR, infrared, and Raman spectroscopy. The DNA in both stems adopt a classical B-form double helical structure with Watson-Crick base pairing and C2'-endo sugar conformation. In addition, the two dG/dC base pairs framing the dA(5)-bulge loop are formed and are stable at least up to 30 degrees C. The five adenine bases of the bulge loop are localized at intrahelical positions within the double helical stems. Stacking on the double helical stem is continued for the first four 5'-adenines in the bulge loop. The total rise (the height) of these four stacked adenines roughly equals the diameter of the double helical stem. The stacking interactions are broken between the last of these four 5'-adenines and the fifth loop adenine at the 3'-end. This 3'-adenine partially stacks on the other stem. The angle between the base planes of the two nonstacking adenines (A10 and A11) in the bulge loop reflects the kinking angle of the global DNA structure. The neighboring cytosines opposite the dA(5)-bulge (being parts of the bulge flanking base pairs) do not stack on one another. This disruption of stacking is characterized by a partial shearing of these bases, such that certain sequential NOEs for this base step are preserved. In the base step opposite the loop, an extraordinary hydrogen bond is observed between the phosphate backbone of the 5'-dC and the amino proton of the 3'-dC in about two-thirds of the conformers. This hydrogen bond probably contributes to stabilizing the global DNA structure. The dA(5)-bulge induces a local kink into the DNA molecule of about 73 degrees (+/-11 degrees ). This kinking angle and the mutual orientation of the two double helical stems agree well with results from fluorescence resonance energy transfer measurements of single- and double-bulge DNA molecules.

Adenine↗
PubMed2002

Influence of d orbital occupation on the binding of metal ions to adenine.

Threshold collision-induced dissociation of M(+)(adenine) with xenon is studied using guided ion beam mass spectrometry. M(+) includes all 10 first-row transition metal ions: Sc(+), Ti(+), V(+), Cr(+), Mn(+), Fe(+), Co(+), Ni(+), Cu(+), and Zn(+). For the systems involving the late metal ions, Cr(+) through Cu(+), the primary product corresponds to endothermic loss of the intact adenine molecule, whereas for Zn(+), this process occurs but to form Zn + adenine(+). For the complexes to the early metal ions, Sc(+), Ti(+), and V(+), intact ligand loss competes with endothermic elimination of purine and of HCN to form MNH(+) and M(+)(C(4)H(4)N(4)), respectively, as the primary ionic products. For Sc(+), loss of ammonia is also a prominent process at low energies. Several minor channels corresponding to formation of M(+)(C(x)H(x)N(x)), x = 1-3, are also observed for these three systems at elevated energies. The energy-dependent collision-induced dissociation cross sections for M(+)(adenine), where M(+) = V(+) through Zn(+), are modeled to yield thresholds that are directly related to 0 and 298 K bond dissociation energies for M(+)-adenine after accounting for the effects of multiple ion-molecule collisions, kinetic and internal energy distributions of the reactants, and dissociation lifetimes. The measured bond energies are compared to those previously studied for simple nitrogen donor ligands, NH(3) and pyrimidine, and to results for alkali metal cations bound to adenine. Trends in these results and theoretical calculations on Cu(+)(adenine) suggest distinct differences in the binding site propensities of adenine to the alkali vs transition metal ions, a consequence of s-dsigma hybridization on the latter.

Adenine↗
PubMed2003

Multiple intermolecular interaction modes of positively charged residues with adenine in ATP-binding proteins.

Adenosine 5'-triphosphate (ATP) plays an essential role in all forms of life. Molecular recognition of ATP in ATP-binding proteins is a subject of great importance for understanding enzymatic mechanisms and for drug design. We have carried out a large-scale data mining of the Protein Data Bank (PDB) to analyze molecular determinants for recognition of ATP, in particular, the adenine base, by ATP-binding proteins. A novel distribution pattern of charged residues around the adenine base was discovered: lysine residues tend to occupy the major groove N7 side of the adenine base, and the arginine residues situate preferentially above or below the adenine bases. Such an arrangement is advantageous because it facilitates multiple modes of intermolecular interactions, that is, cation-pi interactions and a hydrogen bond between lysine and adenine, and cation-pi and pi-pi stacking interactions between arginine and adenine. For the two representative Lys... Adenine and Arg... Adenine interactions, intermolecular interaction energies were subsequently analyzed by means of the supermolecular approach at the MP2 level with solvation free energy correction using the SM5.42R model of Cramer and Truhlar, which gave rise to significant interaction strengths.

Adenine↗
PubMedDate not supplied

Identification of the major lesion from the reaction of an acridine-targeted aniline mustard with DNA as an adenine N1 adduct.

DNA adducts of two acridine-linked aniline half-mustards have been isolated and identified. The compound where the half-mustard is attached to the DNA-targeting acridine moiety by a short linker chain alkylates both double- and single-stranded DNA exclusively at guanine N7, as do the majority of known aromatic and aliphatic nitrogen mustards. The longer-chain analogue, also containing a more reactive half-mustard, shows a strikingly different pattern, alkylating double-stranded DNA to yield primarily (> 90%) the adenine N1 adduct, together with < 10% of the adenine N3 adduct and only trace amounts of the guanine N7 adduct. In the presence of MgCl2 (which is known not to inhibit the interaction of drugs at minor groove sites), the adenine N3 adduct is the major product. The latter compound is the first known aniline mustard (and apparently the first known alkylating agent of any type) to preferentially alkylate adenine at the N1 position in duplex DNA. These results are consistent with previous work [Prakash et al. (1990) Biochemistry 29, 9799-9807], which showed that the preferred site of DNA alkylation by the corresponding long-chain acridine-linked aniline bis-mustards in general was at major groove sites of adenines and identifies the major site of alkylation as adenine N1 and not N7. This selectivity for adenine N1 alkylation is suggested to result from a preference for the acridine mustard side chain of these compounds to project into the major groove following intercalation of the acridine, coupled with structural distortion of the DNA helix to make the N1 positions of adenines adjacent to the intercalation sites more accessible.

Acridines↗
PubMed1975

The effect of butacaine on adenine nucleotide binding and translocation in rat liver mitochondria.

The effect of the local anaesthetic, butacaine, on adenine nucleotide binding and translocation in rat liver mitochondria partially depleted of their adenine nucleotide content was investigated. The range of butacaine concentrations that inhibit adenine nucleotide translocation and the extent of the inhibition are similar to the values obtained for native mitochondria. Butacaine does not alter either the total number of atractyloside-sensitive binding sites of depleted mitochondria, or the affinity of these sites for ADP or ATP under conditions where a partial inhibition of the rate of adenine nucleotide translocation is observed. The data are consistent with an effect of butacaine on the process by which adenine nucleotides are transported across the mitochondrial inner membrane rather than on the binding of adenine nucleotides to sites on the adenine nucleotide carrier. The results are briefly discussed in relation to the use of local anaesthetics in investigations of the mechanism of adenine nucleotide translocation.

4-Aminobenzoic Acid↗
PubMed1998

Adenine nucleotides modulate epithelial wound healing in vitro.

BACKGROUND: Adenine nucleotides have been demonstrated to enhance structural and functional regeneration in experimental renal injury in rats. The mechanism of adenine nucleotide action have not been elucidated. The aim of this study was to characterize the effects of adenine nucleotides on intestinal epithelial wound healing in vitro. METHODS: The effects of adenine nucleotides on cell migration, cell proliferation and cell adhesion were studied in the non-transformed small intestinal epithelial cell line IEC-6 using an in vitro wounding model, a colorimetric BrdU assay and a hexosaminidase adhesion assay. RESULTS: The adenine nucleotides ADP and ATP were found to significantly stimulate epithelial cell restitution (migration) in vitro. Stimulation of epithelial restitution averaged 42% for ADP and 57% for ATP. In addition, adenine nucleotides inhibited the proliferation of rat small intestinal epithelial cells, averaging 56% for ADP and 74% for ATP. Enhancement of intestinal epithelial restitution and inhibition of epithelial cell proliferation by adenine nucleotides were mediated through transforming growth factor (TGF)-beta-independent pathways. CONCLUSION: These findings suggest that adenine nucleotides exert functional effects on intestinal epithelial cell populations and may play a role in the morphogenesis of the gastrointestinal tract and its remodeling after injury.

Adenine Nucleotides↗
PubMedDate not supplied

The renal effect of intravenous adenine in humans.

The purine base, adenine, improves the posttransfusion viability of liquid stored blood. However, adenine in high doses may cause kidney damage becuase of the precipitation in renal tubules of its incoluble metabolite, 2,8-dioxyadenine. Adenine is not licensed for use in the United States because it may be nephrotoxic. In a controlled, randomized, double-blind study, eight human subjects received 10 mg/kg of adenine infused intravenously over one hour, four subjects received 5 mg/kg, and four subjects received no adenine. Renal function tests were performed on each subject before adenine infusion and one day and one week following the infusion. Tests included an assessment of glomerular function (serum creatinine, creatinine clearance, protein excretion), proximal tubular function (amino acid and glucose excretion), and distal tubular function (maximal acidifying and concentrating ability). Plasma and urine levels of adenine and 2,8-dioxyadenine were measured. Renal function tests showed no evidence of kidney damage secondary to adenine.

Adenine↗
PubMed2006

Primary processes underlying the photostability of isolated DNA bases: adenine.

The UV chromophores in DNA are the nucleic bases themselves, and it is their photophysics and photochemistry that govern the intrinsic photostability of DNA. Because stability is related to the conversion of dangerous electronic to less-dangerous vibrational energy, we study ultrafast electronic relaxation processes in the DNA base adenine. We excite adenine, isolated in a molecular beam, to its pipi* state and follow its relaxation dynamics using femtosecond time-resolved photoelectron spectroscopy. To discern which processes are important on which timescales, we compare adenine with 9-methyl adenine. Methylation blocks the site of the much-discussed pisigma* state that had been thought, until now, minor. Time-resolved photoelectron spectroscopy reveals that, although adenine and 9-methyl adenine show almost identical timescales for the processes involved, the decay pathways are quite different. Importantly, we confirm that in adenine at 267-nm excitation, the pisigma* state plays a major role. We discuss these results in the context of recent experimental and theoretical studies on adenine, proposing a model that accounts for all known results, and consider the relationship between these studies and electron-induced damage in DNA.

Adenine↗
PubMed2003

In vitro selection of adenine-dependent hairpin ribozymes.

Adenine-dependent hairpin ribozymes were isolated by in vitro selection from a degenerated hairpin ribozyme population. Two new adenine-dependent ribozymes catalyze their own reversible cleavage in the presence of free adenine. Both aptamers have Mg(2+) requirements for adenine-assisted cleavage similar to the wild-type hairpin ribozyme. Cleavage kinetics studies in the presence of various other small molecules were compared. The data suggest that adenine does not induce RNA self-cleavage in the same manner for both aptamers. In addition, investigations of pH effects on catalytic rates show that both adenine-dependent aptamers are more active in basic conditions, suggesting that they use new acid/base catalytic strategies in which adenine could be involved directly. The discovery of hairpin ribozymes dependent on adenine for their reversible self-cleavage presents considerable biochemical and evolutionary interests because we show that RNA is able to use exogenous reactive molecules to enhance its own catalytic activity. Such a mechanism may have been a means by which the ribozymes of the RNA world enlarged their chemical repertoire.

Adenine↗
PubMed1973

Adenine nucleotide-induced contraction on the inner mitochondrial membrane. II. Effect of bongkrekic acid.

In bovine heart mitochondria bongkrekic acid at concentrations as low as about 4 nmol/mg protein (a) completely inhibits phosphorylation of exogenous adenosine diphosphate (ADP) and dephosphorylation of exogenous adenosine triphosphate (ATP), (b) completely reverses atractyloside inhibition of inner membrane contraction induced by exogenous adenine nucleotides, and (c) decreases the amount of adenine nucleotide required to elicit maximal exogenous adenine nucleotide-induced inner membrane contraction to a level which appears to correspond closely with the concentration of contractile, exogenous adenine nucleotide binding sites Bongkrekic acid at concentrations greater than 4 nmol/mg protein induces inner membrane contraction which seems to depend on the presence of endogenous ADP and/or ATP. The findings appear to be consistent with the interpretations (a) that the inner mitochondrial membrane contains two types of contractile, adenine nucleotide binding sites, (b) that the two sites differ markedly with regard to adenine nucleotide affinity, (c) that the high affinity site is identical with the adenine nucleotide exchange carrier, (d) that the low affinity site is accessible exclusively to endogenous adenine nucleotides and is largely unoccupied in the absence of bongkrekic acid, and (e) that bongkrekic acid increases the affinity of both sites in proportion to the amount of the antibiotic bound to the inner membrane.

Adenine Nucleotides↗
PubMed1968

Some aspects of adenosine triphosphate synthesis from adenine and adenosine in human red blood cells.

1. The synthesis of ATP has been studied in human erythrocytes. Fresh cells showed no net synthesis of ATP when incubated with adenine or adenosine, although labelled adenine was incorporated into ATP in small amounts.2. Cold-stored cells (3-6 weeks old) became progressively depleted of adenine nucleotides but incubation with adenosine or adenine plus inosine restored the ATP concentration to normal within 4 hr. Incorporation of labelled adenine or adenosine into the ATP of incubated stored cells corresponded to net ATP synthesis by these cells.3. Synthesis of ATP from adenosine plus adenine together was 75% derived from adenine and only 25% from adenosine, indicating that nucleotide synthesis from adenine inhibits the simultaneous synthesis of nucleotide from adenosine.

Adenine↗
PubMed1969

Uptake and utilization of S-adenosyl-L-methionine and S-adenosyl-L-homocysteine in an adenine mutant of Saccharomyces cerevisiae.

An adenine mutant of Saccharomyces cerevisiae was able to utilize S-adenosyl-l-methionine (SAM), S-adenosyl-l-homocysteine (SAH), or adenine as sources for growth and ribonucleic acid (RNA) synthesis. Exogenous SAM or SAH was degraded after entering the cell, and the adenine moiety was reutilized in the endogenous synthesis of the thionium compounds. Part of this endogenous synthesis proceeds from an undetermined de novo system of purine synthesis which contributes significantly to the synthesis of SAM and less so to the RNA purines. Some of the methyl groups of exogenous SAM-methyl-(3)H were incorporated into ribosomal and transfer RNA. Methionine partially antagonized this incorporation. The uptake of SAM-adenine-8-(14)C was not affected by the presence of equal quantities of SAH or adenine in the medium. Exogenous SAM affected the uptake of exogenous SAH-adenine-8-(14)C or adenine-8-(14)C. Exogenous SAH inhibited the uptake of exogenous adenine-8-(14)C.

Adenine↗
PubMed2001

Purine salvage to adenine nucleotides in different skeletal muscle fiber types.

Rates of purine salvage of adenine and hypoxanthine into the adenine nucleotide (AdN) pool of the different skeletal muscle phenotype sections of the rat were measured using an isolated perfused hindlimb preparation. Tissue adenine and hypoxanthine concentrations and specific activities were controlled over a broad range of purine concentrations, ranging from 3 to 100 times normal, by employing an isolated rat hindlimb preparation perfused at a high flow rate. Incorporation of [(3)H]adenine or [(3)H]hypoxanthine into the AdN pool was not meaningfully influenced by tissue purine concentration over the range evaluated (approximately 0.10-1.6 micromol/g). Purine salvage rates were greater (P < 0.05) for adenine than for hypoxanthine (35-55 and 20-30 nmol x h(-1) x g(-1), respectively) and moderately different (P < 0.05) among fiber types. The low-oxidative fast-twitch white muscle section exhibited relatively low rates of purine salvage that were approximately 65% of rates in the high-oxidative fast-twitch red section of the gastrocnemius. The soleus muscle, characterized by slow-twitch red fibers, exhibited a high rate of adenine salvage but a low rate of hypoxanthine salvage. Addition of ribose to the perfusion medium increased salvage of adenine (up to 3- to 6-fold, P < 0.001) and hypoxanthine (up to 6- to 8-fold, P < 0.001), depending on fiber type, over a range of concentrations up to 10 mM. This is consistent with tissue 5-phosphoribosyl-1-pyrophosphate being rate limiting for purine salvage. Purine salvage is favored over de novo synthesis, inasmuch as delivery of adenine to the muscle decreased (P < 0.005) de novo synthesis of AdN. Providing ribose did not alter this preference of purine salvage pathway over de novo synthesis of AdN. In the absence of ribose supplementation, purine salvage rates are relatively low, especially compared with the AdN pool size in skeletal muscle.

Adenine Nucleotides↗
PubMed1999

Induction and inhibition of the in vitro N1-oxidation of 9-benzyladenine and isomeric 9-(nitrobenzyl)adenines.

The present study investigated some aspects of the enzymology of the in vitro N1-oxidation of 9-benzyladenine (BA) and isomeric 9-(nitrobenzyl)adenines (NBAs) using various potential inducers and inhibitors of cytochrome P-450 (CYP). When incubated with phenobarbital-induced rabbit hepatic microsomes, the N1-oxidation rates of BA and 9-(4-nitrobenzyl)adenine were about 6- and 2-fold higher than that of the control, respectively; while the N1-oxidation of 9-(2-nitrobenzyl)adenine and 9-(3-nitrobenzyl)adenine was not markedly affected. In contrast, beta-naphthoflavone and Arochlor 1254 showed no inductive effects towards the N1-oxidation of any of these substrates. Using 12 typical CYP inhibitors, it was found that nifedipine (CYP3A inhibitor) and haloperidol (CYP2D inhibitor) showed significant inhibition towards the N1-oxidation of BA and NBAs. Therefore, the N1-oxidation of BA and NBAs is probably catalysed by CYP3A and CYP2D subfamilies. Furthermore, when 9-(4-nitrobenzyl)adenine was incubated with compounds which possessed a certain chemical similarity to the adenine substrate, various degrees of inhibition of N1-oxidation of 9-(4-nitrobenzyl)adenine were observed. These observations allowed a preliminary indication as to the structure-metabolism relationship of 9-substituted adenine derivatives.

Adenine↗
PubMed1984

Biochemical features induced by adenine feeding in rats. Polyuria, electrolyte disorders, and 2,8-dihydroxyadenine deposits.

Levels of sodium, potassium, calcium, and phosphate were examined in rats fed on an adenine diet. Among the electrolytes in the serum, potassium decreased significantly in the adenine-fed group as compared with the control group. A decrease was observed in the level of serum calcium on feeding with an adenine diet. Though a significant decrease in phosphate was noticed in the adenine-fed rats which were kept for 6 to 12 days, the level of phosphate was increased at the 18-30th day as compared with the control group. However, serum sodium concentration was maintained within a relatively narrow range. On the other hand, the animals that continued on the adenine diet showed a significant rise in the urinary excretion of sodium, potassium, and calcium during the test period. Dietary adenine decreased the amount of urinary phosphate. In addition, 2,8-dihydroxyadenine content in kidneys increased during the test period, while a significant increase in the urinary excretion of 2,8-dihydroxyadenine was seen until the 12th day of the feeding period. Furthermore, the results of the present study showed that feeding of adenine to rats produced a significant increase in the urine volume. However, there were no appreciable changes in the water intake of the control and adenine-fed groups throughout the experimental period.

Adenine↗
PubMed2001

[Renal replacement therapy results in correction of plasma and erythrocyte adenine nucleotide abnormalities in patients with chronic renal failure].

High concentration of intraerythrocyte ATP is a common phenomenon in patients with chronic renal failure (CRF). It is likely that this is a result of increased plasma concentration of adenine--one of purine moiety donors which is necessary for ATP synthesis. In the present study we monitored changes of both adenine and intraerythrocyte ATP concentration during renal replacement therapy. We have also estimated the influence of erythropoietin treatment. 4 groups of patients were included into the study: 22 patients with CRF, 22 patients on maintenance hemodialysis treatment (11 patients with EPO therapy), 19 patients after kidney transplantation (7 patients with insufficiency of transplanted kidney) and 26 healthy volunteers served as a control group. The measurements were performed in plasma and erythrocyte extracts using HPLC. Significant decrease of high plasma adenine concentration was observed after both HD session and successful kidney transplantation, however the achieved values were still higher than in healthy volunteers. Kidney transplantation resulted in a permanent decrease of plasma adenine concentration, but along with the deterioration of transplanted kidney function, the plasma adenine concentration reincreased. Also, it started to increase right after HD session had ended. On the other hand, the intraerythrocyte concentration of adenine and ATP after successful kidney transplantation and single HD session came back to normal values. Also in this case, along with the deterioration of transplanted kidney function, both studied parameters reincreased. We have not observed any significant influence of erythropoietin treatment on studied adenine nucleotide concentration in hemodialysis patients. The present study confirms the strong interrelationship between the adenine nucleotide metabolism abnormalities and the advancement of renal failure. The abnormalities intensify along with the disease progression and the renal replacement therapy results in partial their correction.

Adenine↗
PubMed1990

Adenine and guanine nucleotide metabolism during platelet storage at 22 degrees C.

Adenine and guanine nucleotide metabolism of platelet concentrates (PCs) was studied during storage for transfusion at 22 +/- 2 degrees C over a 7-day period using high-pressure liquid chromatography. There was a steady decrease in platelet adenosine triphosphate (ATP) and adenosine diphosphate (ADP), which was balanced quantitatively by an increase in plasma hypoxanthine. As expected, ammonia accumulated along with hypoxanthine but at a far greater rate. A fall in platelet guanosine triphosphate (GTP) and guanosine diphosphate (GDP) paralleled the fall in ATP + ADP. When adenine was present in the primary anticoagulant, it was carried over into the PC and metabolized. ATP, GTP, total adenine nucleotides, and total guanine nucleotides declined more slowly in the presence of adenine than in its absence. With adenine, the increase in hypoxanthine concentration was more rapid and quantitatively balanced the decrease in adenine and platelet ATP + ADP. Plasma xanthine rose during storage but at a rate that exceeded the decline in GTP + GDP. When platelet ATP + ADP was labeled with 14C-adenine at the initiation of storage, half of the radioactivity was transferred to hypoxanthine (45%) and GTP + GDP + xanthine (5%) by the time storage was completed. The isotopic data were consistent with the presence of a radioactive (metabolic) and a nonradioactive (storage) pool of ATP + ADP at the initiation of storage with each pool contributing approximately equally to the decline in ATP + ADP during storage. The results suggested a continuing synthesis of GTP + GDP from ATP + ADP, explaining the slower rate of fall of GTP + GDP relative to the rate of rise of plasma xanthine. Throughout storage, platelets were able to incorporate 14C-hypoxanthine into both adenine and guanine nucleotides but at a rate that was only one fourth the rate of hypoxanthine accumulation. All of these data should be helpful in improving the function and viability of PC as currently stored for 5 days, in devising methods for storage beyond 5 days, and in the development of synthetic media for PC storage.

Adenine Nucleotides↗
PubMed1988

Regulatory effects of adenosine and adenine nucleotides on oxygen radical responses of neutrophils.

Our recent studies have indicated that release of ATP/ADP from platelets causes enhanced O2-. responses in stimulated neutrophils. The current investigations were designed to provide further details of this phenomenon, to determine the structure-function correlates of the adenine compounds, and to assess if the results might be explained by the formation of a single metabolic product of ATP. ATP, ADP, AMP and adenosine enhanced O2-. responses of rat neutrophils stimulated with immune complexes or formyl chemotactic peptide (FMLP) but had no effect on responses of phorbol ester-stimulated neutrophils. Similar results were obtained in human neutrophils stimulated with immune complexes; when FMLP was the agonist, the results were divergent: ATP and ADP enhanced the responses, whereas AMP and adenosine were inhibitory. In structure-function studies, hydrolytically resistant forms of ATP (and other adenine nucleotides) containing blocked or cross-linked phosphate groups were active, suggesting that hydrolysis of these compounds to a common metabolic product is not required for their effects on O2-. responses. In contrast, other chemical modifications of the ribose ring or adenine base of ATP resulted in greatly diminished activity. To further pursue the question of whether metabolism of the adenine compounds via the adenosine pathway was related to the observed effects on O2-. responses, addition to rat neutrophils of inhibitors of adenosine deaminase, S-adenosyl homocysteine hydrolase, or xanthine oxidase failed to reproduce or augment the enhancement effects of the adenine compounds on O2-. responses, suggesting that metabolism of the adenine compounds to a common product may not be a requirement for the observed effects. Although the manner by which the adenine compounds affect O2-. responses is not known, the data suggest that adenosine and adenine nucleotides have important regulatory effects on oxygen radical responses of stimulated neutrophils.

Adenine Nucleotides↗